Chapter 19: Cardiovascular system audio notes part 2

Cardiac Cycle: Phases and Key Concepts

• Overview
  • We examine atrial relaxation and contraction with ventricular filling together, followed by isovolumetric contraction, ventricular ejection, and isovolumetric relaxation. We track AV valves and semilunar valves (open/closed) and the behavior of the atria and ventricles.
  • Chambers: atria contract/relax synchronously on both sides; ventricles also sync. Semilunar valves open only during ejection phase; AV valves open during filling, then close during isovolumetric phases.
  • Electrical activity: ECG waves correspond to mechanical events (P wave with atrial systole, QRS with ventricular contraction, T wave with ventricular/atrial relaxation). Blood movement and chamber pressures correlate with systole (contraction) and diastole (relaxation).

1) Atrial Relaxation and Ventricular Filling

• Valve status at the start
  • AV valves: Open
  • Semilunar valves: Closed
• Chamber states
  • Atria: Diastole (relaxation)
  • Ventricles: Diastole (relaxation); all four chambers relatively low pressure
• Blood movement
  • Blood flows from atria into ventricles (passive filling flow)
  • Pressure: atrial pressure is higher than ventricular pressure during this passive filling phase
• ECG context
  • End of T wave has occurred; P wave is upcoming or just occurring to trigger atrial contraction
• Atrial contraction contribution
  • Passive filling accounts for ~70% of ventricular filling
  • Atrial contraction adds ~30% (active filling) to reach end diastolic volume (EDV)
• End diastolic volume (EDV)
  • EDV = volume in ventricle at end of ventricular diastole, just before ventricular contraction
• Diastole/Systole definitions (recap)
  • Atrial diastole corresponds to atrial relaxation; atrial systole corresponds to atrial contraction
  • Ventricular diastole corresponds to ventricular relaxation; ventricular systole corresponds to ventricular contraction
• Visual indicators
  • In color-coded visuals (as described): chamber green = diastole, pink = systole
• Key statement to remember
  • “Atrial contraction occurs just prior to ventricular contraction” (atrial systole precedes ventricular systole)
• Practical notes
  • The AV valves are open to allow filling; semilunar valves remain closed to prevent backflow into the ventricles
  • Systole/diastole alignment with ECG: P wave precedes atrial contraction; QRS complex precedes ventricular contraction; T wave follows as relaxation begins

2) Isovolumetric Contraction

• What does isovolumetric mean?
  • Iso = same; volumetric change is zero during this phase
• Blood movement
  • No volume change in ventricles; no blood moves into or out of the ventricles
• Valve status at the start
  • AV valves close (first heart sound, S1, due to AV valve closure)
  • Semilunar valves remain closed
• Atria and ventricles behavior
  • Atria: relaxed (diastole); do not participate further in this phase
  • Ventricles: contracting (to build pressure)
• Pressure dynamics
  • Ventricular pressure rises rapidly but remains below arterial trunk pressures initially
  • Purpose: build enough pressure to overcome arterial trunk pressure for ejection
• ECG context
  • QRS complex marks onset of ventricular contraction
• Valve and flow implications
  • All valves closed (no opening) during this phase; no blood moves
• Mechanical goal
  • Pressure in ventricle increases dramatically while volume remains constant
• Clinical/functional note
  • This phase sets up the pressure differential needed for subsequent ejection

3) Ventricular Ejection

• What enables ejection?
  • Ventricular pressure must exceed arterial trunk pressures (pulmonary trunk and aorta) to push blood out
• Valve status
  • Semilunar valves open; AV valves remain closed (to prevent backflow into atria)
• Chambers and flow
  • Ventricles in systole; atria remain in diastole (relaxed)
  • Blood is ejected from ventricles to the pulmonary trunk and aorta
• Pressure profile
  • Ventricular pressure starts lower than arterial trunk pressure and rises to exceed it by the end of ejection
• Blood flow and volumes
  • Stroke volume (SV) is the amount ejected per beat; not all blood is ejected (see EDV/ESV in section below)
• ECG context
  • The QRS complex ends as ejection finishes; we transition toward relaxation
• Valves and papillary muscles
  • AV valves stay closed; semilunar valves open to permit ejection; papillary muscles tense to prevent AV valve prolapse during ventricular contraction
• Conceptual note
  • The arterial trunks (aorta and pulmonary artery) present a back-pressure that the ventricles must overcome to eject blood

4) Isovolumetric Relaxation

• What happens mechanically
  • Ventricles relax after ejection, but no blood moves yet because all valves are closed initially
• Valve status
  • Semilunar valves close (second heart sound, S2, follows the end of ejection)
  • AV valves remain closed at the very start of this phase and then open as ventricular pressure falls below atrial pressure
• Atria and ventricles states
  • Atria: diastole; they begin to refill, but this phase primarily involves the ventricles
  • Ventricles: relaxing; pressure falls rapidly
• Pressure dynamics
  • Ventricular pressure drops below arterial trunk pressures, allowing the semilunar valves to close
  • Ventricular pressure becomes lower than atrial pressure so AV valves can reopen for the next filling phase
• ECG context
  • T wave marks the onset of ventricular repolarization and relaxation, preceding the subsequent filling phase

Valves, Pressures, and Chamber Activity Across the Cycle

• AV valves
  • Open during ventricular filling; close during isovolumetric contraction and remain closed during isovolumetric relaxation until ventricular pressure falls below atrial pressure
• Semilunar valves
  • Closed during atrial contraction and isovolumetric contraction; open during ventricular ejection; close during isovolumetric relaxation
• Chamber states by phase
  • Atria: contract and relax in synchrony; contribute to blood flow into ventricles
  • Ventricles: alternate between filling (diastole) and contraction (systole)
• Pressure relationships
  • During filling: atrial pressure > ventricular pressure
  • During ejection: ventricular pressure > arterial trunk pressure
  • During isovolumetric phases: all valves closed; ventricular pressure rises (isovolumetric contraction) or falls (isovolumetric relaxation) without volume change
• Correlation with ECG waves
  • P wave: atrial depolarization and atrial contraction
  • QRS complex: ventricular depolarization and contraction
  • T wave: ventricular repolarization and relaxation
• End-diastolic volume (EDV) and end-systolic volume (ESV)
  • EDV: blood in ventricle at end of diastole (maximal filling)
  • ESV: blood remaining in ventricle after systole
  • Stroke volume: $SV = EDV - ESV$

Key Measurements and Formulas

• Stroke Volume (SV)
  • $SV = EDV - ESV$
  • Typical values: $EDV \approx 120 \,mL; \ SV \approx 70 \,mL; \ ESV \approx 50 \,mL$
• Cardiac Output (CO)
  • $CO = HR imes SV
  • Typical resting values: $HR \approx 75 \,beats/min; SV \approx 70 \,mL; CO \approx 5.25 \,L/min$
• Cardiac Reserve
  • Increased CO during exercise: healthy non-athlete ~4- to 7-fold increase in CO from resting state; athletes may achieve ~7-fold increase
  • Example: resting CO ~5.25 L/min; exercise CO could rise to ~20–37 L/min depending on fitness level
• EDV/ESV and heart performance
  • EDV reflects venous return and preload; high EDV often yields higher SV via Frank-Starling mechanism
  • ESV reflects how effectively the heart ejected blood; lower ESV implies stronger ejection for a given EDV

Regulation of Heart Rate and Contractility

• Chronotropic effects (heart rate)
  • Positive chronotropic agents increase heart rate; negative chronotropic agents decrease heart rate
  • Primary positive driver: sympathetic nervous system via cardioacceleratory center; involves beta-adrenergic signaling and calcium channel modulation
  • Hormones: thyroid hormone can increase heart rate by upregulating receptors and channels
  • Substances: nicotine, cocaine, caffeine can increase heart rate via sympathetic pathways and calcium-channel effects
  • Mechanism: norepinephrine/epinephrine bind to beta-adrenergic receptors → increased cAMP → opening of calcium channels → faster SA node depolarization
  • Negative chronotropic agents: parasympathetic activity (vagal tone) slows SA node; beta-blockers (prescribed drugs) block beta receptors to reduce heart rate
• Inotropic effects (contractility)
  • Positive inotropes increase contractile force by increasing available intracellular calcium, enhancing cross-bridge formation
  • Negative inotropes decrease contractility by reducing calcium availability; calcium blockers are a common pharmacologic example
  • Calcium’s central role: calcium availability at thick/thin filaments increases cross-bridge cycling and contractile strength
• Venous return, preload, and the Frank-Starling mechanism
  • Venous return: volume of blood returning to the heart; directly affects EDV and preload
  • Preload: stretch of the ventricular wall prior to contraction; higher preload increases cross-bridge formation and SV
  • Frank-Starling law: more venous return → greater ventricular stretch → greater force of contraction → higher SV
  • Exercise effects: muscle pumping and slower heart rate increase venous return and EDV, enhancing CO
  • Reduced venous return (e.g., hemorrhage or low blood volume) reduces EDV and CO
• Afterload
  • Afterload = resistance against which the ventricles must eject blood; higher afterload reduces SV and CO
  • Clinically relevant causes: valvular stenosis, atherosclerosis (narrowed arteries) increase afterload
  • Consequence: increased afterload makes ejection harder and lowers stroke output

Population and Clinical Considerations

• Cardiac output regulation and population differences
  • Sex differences: average CO around 5.25 L/min; males often have higher resting CO due to cardiac size differences
  • Age and body size: smaller hearts or older individuals may have different stroke volumes and heart rates
  • Athletic conditioning: athletes often have larger, stronger hearts, higher stroke volume, and lower resting heart rate (bradycardia) while maintaining CO
  • Bradycardia (resting HR < 60 bpm): common in well-trained athletes; may be normal; in other contexts can indicate hypothyroidism or other conditions
• Infants and exercise capacity
  • Infants typically have higher resting HR (e.g., around 100 bpm) due to smaller heart size and developmental factors
  • To keep CO around typical values, infants have higher HR and smaller stroke volumes (example values used in lectures: stroke volume ~50 mL; CO ~5 L/min; HR ~100 bpm)
• Valvular and perfusion considerations
  • Balanced output: right-sided and left-sided outputs must be equal to prevent edema or congestion
  • Valvular dysfunction (stenosis or regurgitation) disrupts flow, can cause turbulence and abnormal heart sounds
  • Murmurs and auscultation: stethoscope placement and valve operation are used to assess murmurs; abnormal sounds can indicate valvular disease or stenosis
• Clinical relevance of heart sounds
  • S1 (lub): AV valves closing at the start of isovolumetric contraction
  • S2 (dub): semilunar valves closing at the start of isovolumetric relaxation
• Quick anatomical/physiological note
  • The heart’s development includes processes such as the foramen ovale in fetal circulation; this relates to fetal heart structure and not the adult cardiac cycle (topic mentioned for future discussion)

Quick Concepts Review and Practice Prompts

• Which events correspond to atrial systole and ventricular diastole? P wave precedes atrial contraction; following events lead to ventricular filling
• What happens to EDV and SV if venous return increases? EDV increases, preload increases, SV increases via Frank-Starling mechanism
• How does increasing afterload affect SV and CO? SV and CO decrease with higher afterload
• What is the physiological basis for the first and second heart sounds? S1 from AV valve closure; S2 from semilunar valve closure
• How do chronotropic and inotropic agents differ in their effects on the heart? Chronotropic affects rate; inotropic affects contractile force

Connections to Foundational Principles and Real-World Relevance

• Link to perfusion: Cardiac output reflects global perfusion to tissues; adequate CO is necessary for tissue oxygen delivery
• Feedback and homeostasis: Autonomic and hormonal regulation of HR and contractility maintain blood pressure and organ perfusion under varying conditions
• Pathophysiology awareness: Understanding afterload, preload, and contractility helps explain diseases like hypertension, heart failure, and valvular stenosis
• Practical assessment: Clinically, heart sounds and murmurs provide non-invasive clues to valve function and cardiac cycle integrity

Summary Equations and Key Terms

• Cardiac Output: $CO = HR imes SV$
• Stroke Volume: $SV = EDV - ESV$
• Typical resting values (approximate): $HR \approx 75 \,beats/min, \ SV \approx 70 \,mL, \ CO \approx 5.25 \,L/min$
• End-Diastolic Volume (EDV): volume in ventricle at end of diastole
• End-Systolic Volume (ESV): volume in ventricle after systole
• Preload (Frank-Starling): the degree of ventricular stretch at end-diastole, related to EDV
• Afterload: resistance to ejection of blood from the ventricle
• Chronotropic vs Inotropic agents: factors that change heart rate vs factors that change contraction strength
• Frank-Starling law: greater venous return → greater stretch → greater contraction